Fig. 6: PERK modulates activation of NF-κB via STAT3.

a MCF-7:5C cells were treated with E₂ (1 nm), 4-OHT (1 µm), or a combination of them for 24, 48, 72 h. Phosphorylated STAT3 was measured using western blotting. b MCF-7:5C cells were treated with E₂ (1 nm), PERK inhibitor (10 µm), or a combination of them for 48 and 72 h. Phosphorylated STAT3 was measured using western blotting. c The PERK inhibitor blocked STAT3 DNA-binding. MCF-7:5C cells were treated with E₂ (1 nm), PERK inhibitor (10 µm), or a combination of them for 72 h. Nuclear extracts were isolated for EMSA. d MCF-7:5C cells were treated with E₂ (1 nm), STAT3 inhibitor (5 µm), or a combination of them for 72 h. Nuclear extracts were isolated. STAT3 was examined by western blotting. e MCF-7:5C cells were treated with E₂ (1 nm), STAT3 inhibitor (5 µm), or a combination of them for 72 h. Cell lysates were harvested. Phosphorylation of STAT3 was examined by Western blotting. f, g MCF-7:5C cells were treated with E₂ (1 nm), STAT3 inhibitor (5 µm), or a combination of them for 24, 48, and 72 h. STAT3 (f) and NF-κB (g) DNA-binding were measured by EMSA. h MCF-7:5C cells were treated with E₂ (1 nm), STAT3 inhibitor (5 µm), or a combination of them for 72 h. TNFα mRNA expression levels were quantitated by RT-PCR. *P < 0.05 compared with control. i−k MCF-7:5C cells were treated with E₂ (1 nm), PERK inhibitor (10 µm), or a combination of them for 72 h. Nrf2 (i), HMOX1 (j), and HIF-1α (k) mRNA expression levels were quantitated by RT-PCR. *P < 0.05 and **P < 0.001 compared with control